Skip Navigation

Nephrology Dialysis Transplantation 2008 23(4):1112-1115; doi:10.1093/ndt/gfn060
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Schernthaner, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schernthaner, G.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org



Kidney disease in diabetology: lessons from 2007

Guntram Schernthaner

Department of Medicine I, Rudolfstiftung Hospital, Vienna, Austria

Guntram Schernthaner, Rudolfstiftung Hospital, A-1030, Juchgasse 25, Vienna, Austria. Tel: +43-1-71165-2101; Fax: +43-1-7165-2109; E-mail: guntram.schernthaner@meduniwien.ac.at

Keywords: blood pressure control; chronic kidney disease; diabetes; glycaemic control; microalbuminuria

The first 150 words of the full text of this article appear below.



   Introduction
 
Diabetic nephropathy (DNP) is a devasting disorder and is now worldwide the leading cause of end-stage renal failure. This diabetic complication is a complex disease, whereby various genetic and environmental factors determine susceptibility and progression to end-stage renal disease (ESRD). DNP seems to occur as a result of an interaction between metabolic and haemodynamic factors, which activate common pathways that lead to renal damage. In addition, the renin–angiotensin system (RAS) is also an important target for both metabolic and haemodynamic derangements in DNP. High glucose, via various mechanisms such as increased production of oxidative stress and advanced glycation end products, activation of the RAS and protein kinase C and stimulation of the polyol pathway, elicits vascular inflammation and alters gene expression of growth.

Despite the rapid research progress, ideal predictors to assess prospectively, and with high precision, the risk for DNP in individuals with diabetes are still lacking. Unfortunately, currently . . . [Full Text of this Article]

Prevention of diabetic nephropathy by ACE inhibition of ARBs
A low-protein diet reduces proteinuria and inflammation in diabetic patients with macroalbuminuria
Good glycaemic control lowers mortality in diabetic patients on haemodialysis
Improved survival rate in diabetic patients with ESRD
CKD: important risk factor for cardiovascular events and death in type 2 diabetic patients with macrovascular disease
Abnormal lipid profiles in type 1 diabetes with impaired renal function
ADMA predicts cardiovascular events, ESRD and mortality in diabetic patients

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Nephrol Dial TransplantHome page
J. E. Toblli, M. G. Ferrini, G. Cao, D. Vernet, M. Angerosa, and N. F. Gonzalez-Cadavid
Antifibrotic effects of pioglitazone on the kidney in a rat model of type 2 diabetes mellitus
Nephrol. Dial. Transplant., August 1, 2009; 24(8): 2384 - 2391.
[Abstract] [Full Text] [PDF]